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. 2009 Feb;156(4):626–637. doi: 10.1111/j.1476-5381.2008.00066.x

Figure 8.

Figure 8

Oestrogen receptor (ER) antagonist and knockdown of ERβ block the action of g-PPD and g-PPT on HUVECs. Treatment with the ER antagonist, ICI 182,780 (ICI; 10 µmol·L−1), or transfection with a siRNA that silences the ERβ, partially inhibits g-PPD (1 µmol·L−1)- and g-PPT (1 µmol·L−1)-stimulated increases in (A) [Ca2+]i, Western blot analysis of (B) eNOS phosphorylated at Ser-1177 (p-eNOS); (C) summarized data of eNOS phosphorylation (p-eNOS, n = 3); (D) NO generation. DMSO is used here as a solvent control for ICI 182,780 and the non-specific (NS)-siRNA as a control for the siRNA transfection studies. Data are mean ± SD of three experiments. Asterisk (*) indicates a significant difference between control and treatment groups (P ≤ 0.05). [Ca2+]i, intracellular calcium ion concentration; DMSO, dimethyl sulphoxide; eNOS, endothelial nitric oxide synthase; g-PPD, ginsenoside protopanaxadiol; g-PPT, ginsenoside protopanaxatriol; HUVECs, human umbilical vein endothelial cells.

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